During the past decade a large volume of clinical data has been accumulated in our institution that strongly incriminates hypertriglyceridemia as an intermediary between alcohol ingestion and acute pancreatitis. During the past two years data from an isolated ex-vivo perfused canine pancreas have confirmed that triglycerides can initiate pancreatic inflammation, and suggest that the injury is mediated through free fatty acid release from the triglycerides. By continuing to utilize the canine pancreatic preparation, further pathogenic mechanism will be studied and various treatment possibilities evaluated. In addition, the effect of various drugs believed to initiate acute pancreatitis will be evaluated for their effect on the isolated pancreas. Respiratory complications are responsible for a significant proportion of the deaths following severe pancreatitis. Over the past two years we have accumulated information suggesting that hypertriglyceridemia through the release of free fatty acids can cause an isolated ex-vivo perfused ventillated canine pulmonary lobe. Utilizing this preparation, various treatment parameters will be evaluated as to their efficacy of modifying the free fatty acid-induced pulmonary injury. A possible role for phospholipase A in the pathogenesis of respiratory insufficiency in acute pancreatitis will also be evaluated utilizing the isolated canine lobe. Clinical studis will be continued correlating serum phospholipase A, free fatty acid, and triglyceride levels in patients with acute pancreatitis with the respiratory status and arterial blood gases. Finally, we have just concluded a prospective randomized study evaluating atropine in acute pancreatitis, which failed to show any benefit. We now hope to evaluate Cimetadine in a prospective randomized clinical trial.